Background

• SCAD is emerging an important cause of MI particularly in younger women
• SCAD is a nonathersclerotic, nontraumatic cause of ACS and SCD
• high level evidence based guidance is lacking

Epidemiology, Pathophysiology, Genetics

• Typical patient: middle aged woman, few traditional CV risk factors. However, occurs in late teens to 90s. Underlying factors include sex, hormonal fluctuations, arteriopathies, genetics, precipitants (environment, physical, emotional)
  • Women (87-95%)
  • Middle-aged (44-53 years mean age)
  • White (but in all backgrounds as well)
  • May be lacking hypertertension, hyperlipidemia, smoking as risk factors (same as general matched population proportion)
• Prevalence of 4% in all ACS and up to 35% of all ACS in women < 50 years of age
• Pathophysiology
  • acute coronary artery event
  • development of hematoma within tunica media -- separation of the intimal complex from the underlying vessel and compression of the true lumen causing ischemia and AMI
  • two hypotheses
    • (1) "inside-out" --  development of an intimal flap, and blood enters from the true lumen
    • (2) "outside-in" -- hematoma arises de novo in the media from disruption of traversing microvessels. This is MORE LIKELY. Hematomas are PRESSURED and precede development of flap.\
• Genetics
  • associated with some SNPs - related to monogenic changes; +familial risk
  • FMD is associated with SCAD
• Sex hormones
  • Temporally, SCAD has been reported to occur just before or during menstruation while taking hormonal contraceptives and postmenopausal hormone therapy and in women with a history of infertility and/or prior or current treatment for infertility.
  • unknown MOA
• Pregnancy-associated SCAD (P-SCAD) occurs at any time during or after pregnancy
  • 70% occur post-partum, usually within 1st week
  • typically more severe/multivessel presentation
  • comprises up to 1/6 of SCAD overall
  • associated with older age at first childbirth, multigravidas

Presentation and Diagnosis

• Triggers
  • pregnancy, as above
  • extreme physical or emotional stress
• Clinical presentation
  • similar to atherosclerotic ACS
    • chest pain or equivalent symptoms
    • elevated serial biomarkers and ECG findings c/w NSTEMI/STEMI
    • cardiogenic shock, ventricular arrhythmias, SCD
  • therefore, Dx often missed in this patient population
• Diagnosis
  • Catheter-based coronary angiography
    • the primary and typically only necessary modality for diagnosis of SCAD
    • predilection for mid-to-distal coronary arteries, most commonly LAD
    • higher risk features
      • multivessel involvement
      • severe stenosis
      • isolated intramural hematoma
  • Intravascular and noninvasive imaging
    • Not really used. Options are IVUS, OCT, CMR, CCTA

Acute Management of SCAD

Goals are (1) restore/preserve myocardial perfusion and function (2) avoid adverse outcomes related to thrombolysis.

Revascularization

Medical Therapy

• There are no RCTs to guide SCAD-specific pharmacologic management. Treatment is based on sequelae and associated risks
  • LV dysfunction --> GDMT
    • beta blocker associated with less SCAD recurrence
  • PCI with stent --> standard post-PCI DAPT therapy
  • Hypertension --> antihypertensives
  • Hyperlipidemia --> primary prevention guidelines (no association with SCAD)
• Discontinue systemic anticoagulation/GP IIb-IIIa inhibitors once the Dx of SCAD is made, unless there are other indications for systemic anticoagulation or there is an apparent intraluminal thrombus

Anti-thrombotic therapy for SCAD is not guided by strong evidence, but consider DAPT for 2-4 weeks then low-dose ASA for 3-12 months total. Decisions about further therapy should be individualized based on comorbidities and individual risk profile.

References

1. Hayes SN, Tweet MS, Adlam D, et al. Spontaneous Coronary Artery Dissection. Journal of the American College of Cardiology. 2020;76(8):961-984. doi:10.1016/j.jacc.2020.05.084